Ameliorating Potential of Quercetin and Curcumin on Glucose-6-Phosphate Dehydrogenase Expression via miRNAs in Rats with Type 2 Diabetes Mellitus

  • Mahsima Bagheri International Campus of Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  • Ameneh khodarahmi Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
  • Fatemeh Zare Mehrjardi Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
  • Ali Moradi Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
Keywords: Curcumin, G6PD, miRNA, Quercetin, Type 2 diabetes mellitus

Abstract

Background: Type 2 diabetes mellitus (T2DM) is accompanied by a significant risk of oxidative stress. While a link between T2DM and G6PD deficiency has been suggested, their interaction is not precisely understood. Furthermore, emerging evidence suggests an expression association between G6PD and miR-1, miR-122, and miR-206. Given the antioxidant and anti-inflammatory properties of Curcumin (Cur) and Quercetin (Q), This study aimed to assess the effects of curcumin and quercetin on G6PD expression and its correlation with the mentioned microRNA expression in liver, renal, heart, and muscle in rats with T2DM.

Methods: RT-qPCR was employed to determine miR-1, miR-122, miR-206, and G6PD expression.

Results: The findings revealed that curcumin and quercetin treatment elevated G6PD gene expression. Also, the treated groups exhibited down-regulation of miR-1, miR-122, and miR-206 (p<0.05). Furthermore, there was a significant inverse correlation between G6PD and miR-1 in heart, miR-122 in all tissues except renal and miR-206 expression in skeletal muscle and heart (p<0.05).

Conclusion: This study suggests that curcumin and quercetin may prevent the development of T2DM by effectively increasing G6PD expression and reducing miR-1, miR-122, and miR-206 expression.

Published
2025-07-31
Section
Articles